Blair D. Johnson

Perception of fatigue during simulated competition

BACKGROUND Previous studies suggest that the rating of perceived exertion (RPE) increases during steady-state, open-loop exercise in proportion to the relative time to fatigue. This suggests that RPE is scalar and integrates physiological status and homeostatic disturbances. PURPOSE This study assessed the relationship between the rate of change in RPE, and relative distance in time trials at distances of 2.5, 5, and 10 km. It also assessed the rate of change in RPE during 5-km time trials while breathing hypoxic air. METHODS The subjects were well-conditioned cyclists. In part 1, each subject completed habituation time trials, and then randomly ordered time trials at each distance. The category ratio RPE was measured in 10% increments throughout each trial. In part 2, each subject completed three 5-km time trials while breathing different inspired gas mixtures (FiO2 = 0.2093 throughout the trial, FiO2 = 0.15 between 2 and 4 km, and FiO2 = 0.15 between 2.5 and 4 km). RPE was measured at 10% increments. RESULTS In part 1, when RPE was plotted against relative distance, there was no significant difference in the growth of RPE at proportional distances. In part 2, the decrease in power output during the hypoxic segments was sufficient that the growth of RPE was the same at each proportional distance. In both parts of the study, an RPE of 5 (hard) was achieved after 20% of the time trial distance, and an RPE of 8 was achieved after 80% distance. CONCLUSIONS This study supports the hypothesis that RPE increases similarly in relation to relative distance, regardless of the distance performed, and it suggests that the perception of effort has scalar properties.

Mechanotransduction of shear in the endothelium: basic studies and clinical implications.

The endothelium plays an integral role in the development and progression of atherosclerosis. Hemodynamic forces, particularly shear stress, have a powerful influence on endothelial phenotype and function; however, there is no clear consensus on how endothelial cells sense shear. Nevertheless, multiple endothelial cell signal transduction pathways are activated when exposed to shear stress in vitro. The type of shear, laminar or oscillatory, impacts which signal transduction pathways are initiated as well as which subsequent genes are up- or down-regulated, thereby influencing endothelial phenotype and function. Recently, human studies have examined the impact of shear stress and different shear patterns at rest and during exercise on endothelial function. Current evidence supports the theory that augmented exercise-induced shear stress contributes to improved endothelial function following acute exercise and exercise training, whereas retrograde shear initiates vascular dysfunction. The purpose of this review is to examine the current theories on how endothelial cells sense shear stress, to provide an overview on shear stress-induced signal transduction pathways and subsequent gene expression, and to review the current literature pertaining to shear stress and shear patterns at rest as well as during exercise in humans and the related effects on endothelial function.

Normalization of flow-mediated dilation to shear stress area under the curve eliminates the impact of variable hyperemic stimulus

BackgroundNormalization of brachial artery flow-mediated dilation (FMD) to individual shear stress area under the curve (peak FMD:SSAUC ratio) has recently been proposed as an approach to control for the large inter-subject variability in reactive hyperemia-induced shear stress; however, the adoption of this approach among researchers has been slow. The present study was designed to further examine the efficacy of FMD normalization to shear stress in reducing measurement variability.MethodsFive different magnitudes of reactive hyperemia-induced shear stress were applied to 20 healthy, physically active young adults (25.3 ± 0. 6 yrs; 10 men, 10 women) by manipulating forearm cuff occlusion duration: 1, 2, 3, 4, and 5 min, in a randomized order. A venous blood draw was performed for determination of baseline whole blood viscosity and hematocrit. The magnitude of occlusion-induced forearm ischemia was quantified by dual-wavelength near-infrared spectrometry (NIRS). Brachial artery diameters and velocities were obtained via high-resolution ultrasound. The SSAUC was individually calculated for the duration of time-to-peak dilation.ResultsOne-way repeated measures ANOVA demonstrated distinct magnitudes of occlusion-induced ischemia (volume and peak), hyperemic shear stress, and peak FMD responses (all p < 0.0001) across forearm occlusion durations. Differences in peak FMD were abolished when normalizing FMD to SSAUC (p = 0.785).ConclusionOur data confirm that normalization of FMD to SSAUC eliminates the influences of variable shear stress and solidifies the utility of FMD:SSAUC ratio as an index of endothelial function.

Postprandial lipaemia, oxidative stress and endothelial function: a review

Aims:  Postprandial lipaemia‐induced endothelial dysfunction is felt to be mediated by increases in oxidative stress. In this review, we have examined the cross‐sectional relationships found among these three variables.

Adjusting flow-mediated dilation for shear stress stimulus allows demonstration of endothelial dysfunction in a population with moderate cardiovascular risk

Background/Aims: Although normalization of brachial artery flow-mediated dilation (FMD) to individual shear stress (FMD:shear stress ratio) has been proposed to improve this measure of endothelial function, the clinical utility of FMD normalization has not yet been demonstrated. We tested (1) whether following conventional 5-min forearm occlusion, the FMD:shear stress ratio would discriminate a population with moderate cardiovascular risk (MR) from a low-risk (LR) population, and (2) whether the dose-response profile relating shear stress to FMD would be different between the 2 populations. Methods: Five different magnitudes of reactive hyperemia-induced shear stress were applied to 20 MR and 20 LR subjects by manipulating forearm cuff occlusion duration. Brachial artery diameters and velocities were measured via high-resolution ultrasound. To quantify the hyperemic stimulus, shear stress area under the curve was individually calculated for the duration of time-to-peak dilation. Results: Following 5-min of forearm occlusion, FMD:shear stress ratio (p = 0.041), but not FMD (p = 0.286), discriminated MR from LR. The slope of the shear stress-FMD regression line was lower in MR compared to the LR (p <0.001). Conclusion: The FMD:shear stress ratio distinguished reduced endothelial function in a population with MR. The dose-response profile of the shear stress-FMD relationship appears to differ between populations of distinct cardiovascular risk.

ACCURACY OF PREDICTION EQUATIONS FOR DETERMINING ONE REPETITION MAXIMUM BENCH PRESS IN WOMEN BEFORE AND AFTER RESISTANCE TRAINING

Mayhew, JL, Johnson, BD, LaMonte, MJ, Lauber, D, and Kemmler, W. Accuracy of prediction equations for determining one repetition maximum bench press in women before and after resistance training. J Strength Cond Res 22(5): 1570-1577, 2008-Repetitions to fatigue (RTF) using less than a 1 repetition maximum (1RM) load (RepWt) have been shown to be a good predictor of 1RM strength in men, but such information is scarce in women. The purpose of this study was to evaluate the accuracy of current prediction equations to estimate 1RM bench press performance and to determine whether resistance training changes the capability to predict 1RM from muscular endurance repetitions in young women. Members (n = 103) of a required wellness course were measured for 1RM bench press and RTF using randomly assigned percentages between 60% and 90% of the 1RM (RepWt) before and after 12 weeks of progressive resistance training. The %1RM used to perform RTF remained the same for each individual after training (75.6% ± 10.3%) as before. One repetition maximum bench press increased significantly after training (28% ± 21%). Although the change in the group average for RTF (0.6 ± 6.1) was not significant, the correlation between pretraining and posttraining RTF was moderate (r = 0.66; p < 0.01), and individual differences in percentage change in RTF were substantial (27% ± 99%). The percentage change in 1RM was not significantly related to initial 1RM (r = −0.05), but it was negatively related to the change in RTF (r = −0.40; p < 0.01). Prediction equations were more accurate in the pretraining and posttraining conditions, in which fewer than 10 RTF were used. Resistance training may alter the relationship between strength and muscle endurance across a wide range of RTF in young women without compromising the accuracy of predicting maximal strength.

Sitting and endothelial dysfunction: The role of shear stress

Summary Sedentary activity is a modifiable life-style behavior and a key component in the etiology of atherosclerotic cardiovascular disease (ACVD). US adults and children spend more than half their waking time in sedentary pursuits. Sedentary activity has been shown to result in impaired insulin sensitivity, impaired metabolic function and attenuated endothelial function, which are classic markers of ACVD. Sedentary activity is defined as ‘sitting without otherwise being active.’ This behavior promotes reduced muscular activity of the lower extremities which decreases leg blood flow, increases blood pooling in the calf, augments mean arterial pressure, and deforms arterial segments resulting in low mean shear stress (SS). SS activates distinct physiological mechanisms which have been proposed to be protective against ACVD; specifically through a SS-induced endothelium-derived nitric oxide mechanism. Reduced bioavailability of nitric oxide creates a pro-oxidant milieu resulting in increased oxidative stress. There is sufficient evidence which demonstrates that endothelial function is attenuated in the presence of oxidative stress. Sedentary activity results in low SS in the lower extremities which may result in increased oxidative stress and impaired endothelial function. This review furthers the use of sitting as model to study the effects of inactivity, discusses possible physiological mechanisms and suggests future directions.

Reductions in central venous pressure by lower body negative pressure or blood loss elicit similar hemodynamic responses

The purpose of this study was to compare hemodynamic and blood analyte responses to reduced central venous pressure (CVP) and pulse pressure (PP) elicited during graded lower body negative pressure (LBNP) to those observed during graded blood loss (BL) in conscious humans. We hypothesized that the stimulus-response relationships of CVP and PP to hemodynamic responses during LBNP would mimic those observed during BL. We assessed CVP, PP, heart rate, mean arterial pressure (MAP), and other hemodynamic markers in 12 men during LBNP and BL. Blood samples were obtained for analysis of catecholamines, hematocrit, hemoglobin, arginine vasopressin, and blood gases. LBNP consisted of 5-min stages at 0, 15, 30, and 45 mmHg of suction. BL consisted of 5 min at baseline and following three stages of 333 ml of hemorrhage (1,000 ml total). Individual r(2) values and linear regression slopes were calculated to determine whether the stimulus (CVP and PP)-hemodynamic response trajectories were similar between protocols. The CVP-MAP trajectory was the only CVP-response slope that was statistically different during LBNP compared with BL (0.93 ± 0.27 vs. 0.13 ± 0.26; P = 0.037). The PP-heart rate trajectory was the only PP-response slope that was statistically different during LBNP compared with BL (-1.85 ± 0.45 vs. -0.46 ± 0.27; P = 0.024). Norepinephrine, hematocrit, and hemoglobin were all lower at termination in the BL protocol compared with LBNP (P < 0.05). Consistent with our hypothesis, LBNP mimics the hemodynamic stimulus-response trajectories observed during BL across a significant range of CVP in humans.

Vitamin C prevents the acute decline of flow-mediated dilation after altered shear rate patterns

Oscillatory and retrograde shear rate (SR) impairs endothelial function, potentially through shear-induced oxidative stress. We tested the hypothesis that acute vitamin C supplementation would prevent the attenuation of brachial artery flow-mediated dilation (FMD) after a period of augmented oscillatory and retrograde SR. Twelve healthy men (aged 26 ± 3 years) participated in two 30-min study visits in which one arm was subjected to increased oscillatory and retrograde SR, using 60 mm Hg of forearm cuff compression, and the contralateral arm served as the control. Subjects ingested capsules containing either placebo (sucrose) or vitamin C at 90 and 120 min (1000 mg total vitamin C) prior to cuff compression periods in a randomized placebo-controlled double-blind crossover study. Oscillatory and retrograde SR in the cuffed arms increased during the compression periods in the placebo and vitamin C study visits (p < 0.01 for both), with no difference between studies (p > 0.05). Antegrade SR remained unchanged throughout the compression periods (p > 0.05), and mean SR was lower in the cuffed arm than in the control arm for both study visits (p < 0.05). FMD decreased after cuff compression in the placebo cuffed arm (precompression vs. postcompression, 5.2% ± 1.4% vs. 3.5% ± 1.4%; p < 0.05), but remained unchanged after vitamin C therapy in the cuffed arm (precompression vs. postcompression, 5.3% ± 2.4% vs. 5.7% ± 2.6%; p > 0.05). No FMD changes were observed in the control arm for either study visit (p > 0.05). These data demonstrate that acute vitamin C supplementation prevents the attenuation of FMD due to altered SR patterns, suggesting that oxidative stress contributes to the oscillatory and retrograde SR-induced impairment of FMD.

Brachial Artery Flow-mediated Dilation Following Exercise with Augmented Oscillatory and Retrograde Shear Rate

BackgroundAcute doses of elevated retrograde shear rate (SR) appear to be detrimental to endothelial function in resting humans. However, retrograde shear increases during moderate intensity exercise which also enhances post-exercise endothelial function. Since SR patterns differ with the modality of exercise, it is important to determine if augmented retrograde SR during exercise influences post-exercise endothelial function. This study tested the hypothesis that (1) increased doses of retrograde SR in the brachial artery during lower body supine cycle ergometer exercise would attenuate post-exercise flow-mediated dilation (FMD) in a dose-dependent manner, and (2) antioxidant vitamin C supplementation would prevent the attenuated post-exercise FMD response.MethodsTwelve men participated in four randomized exercise sessions (90 W for 20 minutes) on separate days. During three of the sessions, one arm was subjected to increased oscillatory and retrograde SR using three different forearm cuff pressures (20, 40, 60 mmHg) (contralateral arm served as the control) and subjects ingested placebo capsules prior to exercise. A fourth session with 60 mmHg cuff pressure was performed with 1 g of vitamin C ingested prior to the session.ResultsPost-exercise FMD following the placebo conditions were lower in the cuffed arm versus the control arm (arm main effect: P < 0.05) and without differences between cuff pressures (20 mmHg: 5.7 ± 2.2%; 40 mmHg: 4.7 ± 1.3%; 60 mmHg: 5.4 ± 2.4%) (P > 0.05). Following vitamin C treatment, post-exercise FMD in the cuffed and control arm increased from baseline (P < 0.05) but were not different (control: 7.1 ± 3.5% vs. cuffed: 6.6 ± 3.3%) (P > 0.05).ConclusionsThese results indicate that augmented oscillatory and retrograde SR in non-working limbs during lower body exercise attenuates post-exercise FMD without an evident dose–response in the range of cuff pressures evaluated. Vitamin C supplementation prevented the attenuation of FMD following exercise with augmented oscillatory and retrograde SR suggesting that oxidative stress contributes to the adverse effects of oscillatory and retrograde shear during exercise on FMD.